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Advancements in Inflammatory and Oxidative Disease Research
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Advancements in Inflammatory and Oxidative Disease Research

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 1738

Special Issue Editor

Dr. Sandra Barbalho

E-Mail Website
Guest Editor
Laboratory for Systematic Investigations of Diseases, Department of Biochemistry and Pharmacology, School of Medicine, University of Marília (UNIMAR), Marília 17525-902, SP, Brazil
Interests: inflammatory diseases; cardiovascular diseases; neurodegenerative diseases; inflammation; medicinal plants; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Excessive inflammation and oxidative stress are detrimental to our body’s homeostasis. Therefore, we warmly invite you to submit your valuable contributions and papers to our Special Issue in the International Journal of Molecular Sciences. Inflammatory and oxidative diseases span a wide range of medical specialties, including endocrinology, neurology, gastroenterology, pulmonology, and rheumatology. Interdisciplinary research is especially relevant in diseases such as diabetes, which affect multiple organs beyond the pancreas, contributing to complications encompassing diabetic cardiomyopathy and diabetic nephropathy. Investigating novel approaches to inflammatory and oxidative diseases, disease progression, pharmacological prevention and intervention strategies is paramount. Our Special Issue welcomes original articles as well as reviews. We also invite you to submit studies on using medicinal plants and bioactive compounds as well as established, novel, or yet to be explored drugs as an intervention. Papers using interdisciplinary approaches to inflammatory and oxidative diseases are also welcome. Clinical human trials, preclinical cellular and animal studies, and special critical and systematic reviews with breakthrough advances will receive special attention.

This Special Issue is supervised by Dr. Sandra Barbalho and assisted by our Guest Editor Assistant Dr. Lucas Fornari Laurindo, Department of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR). Thank you for considering our Special Issue for your research. We appreciate your interest and look forward to receiving your papers.

Dr. Sandra Barbalho
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetes
  • cancer
  • neurological diseases
  • inflammation
  • oxidative stress
  • endocrinology
  • gastroenterology
  • pulmonology
  • rheumatology
  • cardiology
  • neurology
  • nephrology
  • dermatology

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Published Papers (2 papers)

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Research

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18 pages, 1733 KB  
Article
Lysophosphatidylethanolamine Degradation Associated with Upregulation of Pnpla6/7 in a Murine Model of Metabolic Dysfunction-Associated Steatohepatitis
by Nao Inoue, Hsin-Jung Ho, Siddabasave Gowda B. Gowda, Miki Eguchi, Minato Masamura-Takeuchi, Hitoshi Chiba and Shu-Ping Hui
Int. J. Mol. Sci. 2026, 27(4), 1869; https://doi.org/10.3390/ijms27041869 - 15 Feb 2026
Viewed by 295
Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a form of fatty liver disease characterized by fat accumulation, hepatic inflammation, and fibrosis. Lysophosphatidylethanolamine (LPE), a partially deacylated product of phosphatidylethanolamine, plays significant roles in anti-inflammatory responses and mitochondrial homeostasis. Although serum LPE levels are reduced in [...] Read more.
Metabolic dysfunction-associated steatohepatitis (MASH) is a form of fatty liver disease characterized by fat accumulation, hepatic inflammation, and fibrosis. Lysophosphatidylethanolamine (LPE), a partially deacylated product of phosphatidylethanolamine, plays significant roles in anti-inflammatory responses and mitochondrial homeostasis. Although serum LPE levels are reduced in patients with MASH, the underlying mechanisms remain unclear. In this study, we investigated LPE metabolism using liquid chromatography–tandem mass spectrometry and protein expressions in MASH mice. Male C57BL/6J mice were fed a high-fat, high-cholesterol, and cholic acid diet, along with 2% hydroxypropyl-β-cyclodextrin in drinking water (HFCC/CDX) for three weeks to induce MASH. LPE was primarily distributed in the liver and kidneys, with lower levels in the white adipose tissue. HFCC/CDX mice exhibited accumulation of cholesterols and oxidized triglycerides, accompanied by inflammation and fibrosis in the liver. In the plasma and liver of HFCC/CDX mice, most LPE species were decreased and showed negative correlations with hepatic inflammation, with the exception of LPE 18:1. Mechanistically, enhanced degradation of LPE to glycerophosphorylethanolamine was associated with upregulation of Pnpla6/7 in the liver. These findings suggest that Pnpla6/7-driven LPE catabolism is contributing to LPE depletion. This study provides a new perspective to understand the association between disrupted phospholipid metabolism and MASH pathogenesis. Full article
(This article belongs to the Special Issue Advancements in Inflammatory and Oxidative Disease Research)
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Review

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19 pages, 1156 KB  
Review
The Pleiotropic Influence of Cannabidiol and Tetrahydrocannabinol on Inflammatory Biomarkers: A Systematic Review and Meta-Analytical Synthesis
by Bruno Moreira Candeloro, Camila M. de Oliveira, Fabiana Veronez Martelato Gimenez, Marianne P. C. N. Barbosa, Beatriz Paiva Soares, Ana C. F. Ruiz, Derfel R. M. A. Folegatti, Sandra Maria Barbalho, Nancy S. Oliveira, Andrey A. Porto, David Matthew Garner, Fernando H. Sousa and Vitor E. Valenti
Int. J. Mol. Sci. 2025, 26(23), 11618; https://doi.org/10.3390/ijms262311618 - 30 Nov 2025
Cited by 2 | Viewed by 1043
Abstract
Preclinical data suggest that cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC) modulate inflammatory pathways (e.g., NLRP3, NF-κB, and PPAR-γ), but clinical translation into consistent changes in circulating biomarkers remains ambiguous. Two reviewers independently screened the studies, extracted data, and assessed risk of bias with RoB-2. [...] Read more.
Preclinical data suggest that cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC) modulate inflammatory pathways (e.g., NLRP3, NF-κB, and PPAR-γ), but clinical translation into consistent changes in circulating biomarkers remains ambiguous. Two reviewers independently screened the studies, extracted data, and assessed risk of bias with RoB-2. Random-effects meta-analyses (RevMan 5.4.1) formed standardized mean differences (SMD) or mean differences (MD) as appropriate. The certainty of evidence was graded by means of GRADE. Thirteen studies satisfied inclusion criteria; meta-analyses were feasible for IL-6 (four studies, n ≈ 129 per arm), IL-8 (two studies, n ≈ 78 per arm), IL-10 (two studies, n ≈ 92 per arm), and TNF-α (three studies, n ≈ 105 per arm). Pooled estimates favored CBD but were trivial and imprecise: IL-6 SMD −0.17 (95% CI −0.56 to 0.23; p = 0.41; I2 = 55%); IL-8 SMD −0.30 (95% CI −0.62 to 0.01; p = 0.06; I2 = 0%); IL-10 SMD −0.10 (95% CI −0.83 to 0.63; p = 0.79; I2 = 81%); and TNF-α SMD −0.09 (95% CI −0.45 to 0.27; p = 0.62; I2 = 33%). Individual trials reported reductions in biomarkers in high-exposure or diseased populations. GRADE ratings were as follows: IL-6 very low, IL-8 moderate, IL-10 low, and TNF-α moderate. Current RCT evidence demonstrates inconsistent, often trivial effects of phytocannabinoid interventions on circulating inflammatory biomarkers. Full article
(This article belongs to the Special Issue Advancements in Inflammatory and Oxidative Disease Research)
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